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Brief Report

Cecum axis (CecAx) preservation reveals physiological and pathological gradients in mouse gastrointestinal epithelium

, , , , , , , & ORCID Icon show all
Article: 2185029 | Received 16 Nov 2022, Accepted 17 Feb 2023, Published online: 05 Mar 2023
 

ABSTRACT

The mouse cecum has emerged as a model system for studying microbe-host interactions, immunoregulatory functions of the microbiome, and metabolic contributions of gut bacteria. Too often, the cecum is falsely considered as a uniform organ with an evenly distributed epithelium. We developed the cecum axis (CecAx) preservation method to show gradients in epithelial tissue architecture and cell types along the cecal ampulla-apex and mesentery-antimesentery axes. We used imaging mass spectrometry of metabolites and lipids to suggest functional differences along these axes. Using a model of Clostridioides difficile infection, we show how edema and inflammation are unequally concentrated along the mesenteric border. Finally, we show the similarly increased edema at the mesenteric border in two models of Salmonella enterica serovar Typhimurium infection as well as enrichment of goblet cells along the antimesenteric border. Our approach facilitates mouse cecum modeling with detailed attention to inherent structural and functional differences within this dynamic organ.

Acknowledgments

Core Services performed through the Digestive Disease Research Center were supported by NIH grant P30DK058404. We acknowledge the Translational Pathology Shared Resource supported by NCI/NIH Cancer Center Support Grant 5P30 CA68485-19. The Imaging Mass Spectrometry work was performed in the Imaging Mass Spectrometry Core (IMSC) at Vanderbilt University.

Disclosure statement

We have no financial disclosures or conflicts of interest. The contents do not represent the views of the U.S. Department of Veterans Affairs or the United States Government.

Supplementary data

Supplemental data for this article can be accessed online at https://doi.org/10.1080/19490976.2023.2185029

Additional information

Funding

The work was supported by the Howard Hughes Medical Institute through the James H. Gilliam Fellowships for Advanced Study program [GT15104]; National Institute of Allergy and Infectious Diseases [AI957555]; National Institute of Allergy and Infectious Diseases [AI168302]; U.S.Department of Veterans Affairs [BX005699]; U.S. Department of Veterans Affairs [BX002943]